The tenth European Consensus Conference on Hyperbaric Medicine took place in Lille, France, 14-16 April, 2016, attended by a large delegation of experts from Europe and elsewhere. The focus of the meeting was the revision of the European Committee on Hyperbaric Medicine (ECHM) list of accepted indications for hyperbaric oxygen treatment (HBOT), based on a thorough review of the best available research and evidence-based medicine (EBM). For this scope, the modified GRADE system for evidence analysis, together with the DELPHI system for consensus evaluation, were adopted.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02).

Introduction: The risk for decompression sickness (DCS) after hyperbaric exposures (such as SCUBA diving) has been linked to the presence and quantity of vascular gas emboli (VGE) after surfacing from the dive. These VGE can be semi-quantified by ultrasound Doppler and quantified via precordial echocardiography. However, for an identical dive, VGE monitoring of divers shows variations related to individual susceptibility, and, for a same diver, dive-to-dive variations which may be influenced by pre-dive pre-conditioning. These variations are not explained by currently used algorithms. In this paper, we present a new hypothesis: individual metabolic processes, through the oxygen window (OW) or Inherent Unsaturation of tissues, modulate the presence and volume of static metabolic bubbles (SMB) that in turn act as precursors of circulating VGE after a dive.

BACKGROUND: Using ultrasound imaging, vascular gas emboli (VGE) are observed after asymptomatic scuba dives and are considered a key element in the potential development of decompression sickness (DCS). Diving is also accompanied with vascular dysfunction, as measured by flow-mediated dilation (FMD). Previous studies showed significant intersubject variability to VGE for the same diving exposure and demonstrated that VGE can be reduced with even a single pre-dive intervention. Several preconditioning methods have been reported recently, seemingly acting either on VGE quantity or on endothelial inflammatory markers.